4 ms·

>We might know that catecholamines are pushed out of the presynaptic neurons, but how/why does that treat conditions like ADHD, Narcolepsy, Binge-Eating Disorde

by serf 2y ago

>We might know that catecholamines are pushed out of the presynaptic neurons, but how/why does that treat conditions like ADHD, Narcolepsy, Binge-Eating Disorder, etc.? those disorders are often characterized by inappropriate dopamine/norepinepherine levels. if you push more catecholamines into availability, while also reducing the ability for them to be re-uptaked by their associated transport chains, then the patient begins to edge towards a more normal saturation level of the deficit chemicals.

gruez 2y ago
That doesn't explain why SSRIs take weeks to work, rather than hours/days.
- solumunus 2y ago
  They were talking about amphetamines.
- Jarwain 2y ago
  My understanding is that with SSRIs it's not the drug itself that helps but rather the repercussions of developing a "tolerance" to the drug. Trying to remember what a neuroscience friend of mine said; your brain, like your body, tries to reach some sort of homeostasis. Inhibiting the reuptake of serotonin results in there being more serotonin in the brain, resulting in your brain changing somehow to handle this serotonin. These changes take time to develop, thus the delay on the impact of ssris. Generally, consistent use of any drug will cause these longer term changes in the brain. Since your body is trying to find homeostasis, these changes reduce the impact of the acute effect of the drug, thus the experience of tolerance. The experience of withdrawal is a side effect of having these changes without the acute effect of the drug.
  - alan-hn 2y ago
    Is the overload of presynaptic serotonin receptors that ends up causes endocytosis of those very receptors. The purpose of these receptors is to help regulate vesicular release of serotonin into the synapse by shutting down release when too much is detected. Less of those receptors means more serotonin in the synapse after long periods of treatment. The current overall theory (iirc) is that this helps to drive BDNF upregulation which is a neuronal growth factor that helps to drive more dendrite and bouton formation leading to new and more robust network connections
bhouston 2y ago
> those disorders are often characterized by inappropriate dopamine/norepinepherine levels. Those are secondary effects of underlying issues in ADHD, Binge-Eating, etc. The core issue is something not working well, such as in ADHD, the brain may have smaller prefrontal cortex regions (or less connected, etc) and thus have problem with self-regulation. You can sort of work around this by boosting dopamine, but it is working around the issue. It is akin to an engine that is under powered so we figure you show to press the gas pedal harder (dopamine increases focus/effort/alert, so it is like pressing on the gas.) But the core issue is that the engine is underpowered in comparison to others. And it may be underpowered for a large variety of very specific reasons, including genetics (controlling development, or resistance to stressors), physical trauma, sleep, etc.
hirvi74 2y ago
> those disorders are often characterized by inappropriate dopamine/norepinepherine levels. My understanding is that is still hypothetical at this point, albeit the leading hypothesis. Personally, I think that ADHD is just an abstraction for a set of behaviors. I am not trying to downplay its severity, it's caused me undue suffering, but my point being that I believe there are multiple etiologies that have fairly similar symptoms. After all, stimulants have a wide variance in efficacy for people with ADHD, and there are plenty of medications that are even non-stimulants, so I think that should be a sign that there is much more to this disorder(s) than just dopamine and norepinephrine. But hey, what do I know?

by serf 2y ago

gruez 2y ago

That doesn't explain why SSRIs take weeks to work, rather than hours/days.

solumunus 2y ago
They were talking about amphetamines.
Jarwain 2y ago
My understanding is that with SSRIs it's not the drug itself that helps but rather the repercussions of developing a "tolerance" to the drug. Trying to remember what a neuroscience friend of mine said; your brain, like your body, tries to reach some sort of homeostasis. Inhibiting the reuptake of serotonin results in there being more serotonin in the brain, resulting in your brain changing somehow to handle this serotonin. These changes take time to develop, thus the delay on the impact of ssris. Generally, consistent use of any drug will cause these longer term changes in the brain. Since your body is trying to find homeostasis, these changes reduce the impact of the acute effect of the drug, thus the experience of tolerance. The experience of withdrawal is a side effect of having these changes without the acute effect of the drug.
- alan-hn 2y ago
  Is the overload of presynaptic serotonin receptors that ends up causes endocytosis of those very receptors. The purpose of these receptors is to help regulate vesicular release of serotonin into the synapse by shutting down release when too much is detected. Less of those receptors means more serotonin in the synapse after long periods of treatment. The current overall theory (iirc) is that this helps to drive BDNF upregulation which is a neuronal growth factor that helps to drive more dendrite and bouton formation leading to new and more robust network connections

bhouston 2y ago

> those disorders are often characterized by inappropriate dopamine/norepinepherine levels. Those are secondary effects of underlying issues in ADHD, Binge-Eating, etc. The core issue is something not working well, such as in ADHD, the brain may have smaller prefrontal cortex regions (or less connected, etc) and thus have problem with self-regulation. You can sort of work around this by boosting dopamine, but it is working around the issue. It is akin to an engine that is under powered so we figure you show to press the gas pedal harder (dopamine increases focus/effort/alert, so it is like pressing on the gas.) But the core issue is that the engine is underpowered in comparison to others. And it may be underpowered for a large variety of very specific reasons, including genetics (controlling development, or resistance to stressors), physical trauma, sleep, etc.

hirvi74 2y ago

> those disorders are often characterized by inappropriate dopamine/norepinepherine levels. My understanding is that is still hypothetical at this point, albeit the leading hypothesis. Personally, I think that ADHD is just an abstraction for a set of behaviors. I am not trying to downplay its severity, it's caused me undue suffering, but my point being that I believe there are multiple etiologies that have fairly similar symptoms. After all, stimulants have a wide variance in efficacy for people with ADHD, and there are plenty of medications that are even non-stimulants, so I think that should be a sign that there is much more to this disorder(s) than just dopamine and norepinephrine. But hey, what do I know?